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目的:研究重度子痫前期(PE)患者血清MPO及胎盘组织中MPO mRNA表达水平变化与PE发病的关系,探讨糖脂代谢异常及氧化应激在PE病理生理机制中的可能作用。方法:选取60例重度PE孕妇,按发病时孕周不同分为早发型PE组(孕周<34周)和晚发型PE组(孕周≥34周)各30例。另选取同期健康晚期妊娠孕妇60例,分为对照1组(孕周<34周)和对照2组(孕周≥34周)各30例。采用实时荧光定量PCR技术检测胎盘组织中MPO mRNA表达水平;ELISA法检测血清MPO水平。检测患者血压、血脂、血糖、胰岛素水平等指标,进行相关性分析。结果:PE组的血清MPO水平高于对照组(P<0.05),且早发型高于晚发型PE组(P<0.05);但对照组间比较无差异(P>0.05)。PE组的血清TC、TG、LDL、FINS、HOMA-IR分别高于对照组(P<0.05),HDL水平低于对照组(P<0.05);但PE组间比较及对照组间比较,均无差异(P>0.05)。PE组的脐血MPO水平、胎盘组织中MPO mRNA表达水平均高于对照2组(P<0.05),且早发型高于晚发型组(P<0.05)。PE组的血清MPO水平与TG、HoMA-IR、FINS、胎盘组织MPO mRNA表达水平均呈正相关(r=0.557、0.615;0.694、0.511;0.766、0.717;0.696、0.695),与血HDL呈负相关(r=-0.697,-0.576);对照2组则无相关性。结论:MPO可能参与了PE的病理生理过程。胎盘组织中MPO mRNA表达水平升高可能是血清MPO水平升高的重要原因。PE患者血脂代谢异常及胰岛素抵抗增加与血清MPO水平升高有关,它们可能参与了血清MPO水平升高后促发PE的氧化应激的病理生理过程。
Objective: To study the relationship between MPO mRNA expression in MPO and placental tissue in patients with severe preeclampsia (PE) and the pathogenesis of PE, and to explore the possible role of abnormal glucose and lipid metabolism and oxidative stress in the pathophysiology of PE. Methods: 60 pregnant women with severe PE were divided into premature PE group (<34 weeks gestational age) and 30 cases of late onset PE group (gestational age> 34 weeks) according to their gestational age. Another 60 healthy pregnant women of the same period were enrolled in this study. They were divided into control group 1 (34 weeks of gestational age) and control group 2 (30 weeks of gestational age≥34 weeks). Real-time fluorescent quantitative PCR was used to detect the expression of MPO mRNA in placenta. The level of MPO was detected by ELISA. Blood pressure, blood lipids, blood glucose, insulin levels and other indicators were measured for correlation analysis. Results: The level of serum MPO in PE group was higher than that in control group (P <0.05), and the rate of early onset in early PE was higher than that in late onset PE (P <0.05). There was no significant difference between the two groups (P> 0.05). The levels of serum TC, TG, LDL, FINS and HOMA-IR in PE group were higher than those in control group (P <0.05), but HDL levels were lower in control group (P <0.05) No difference (P> 0.05). MPO levels in cord blood and MPO mRNA expression in placenta of PE group were higher than those in control group 2 (P <0.05), and those in early-onset group were higher than those in late-onset group (P <0.05). Serum levels of MPO in PE group were positively correlated with TG, HoMA-IR, FINS and placental MPO mRNA levels (r = 0.557,0.615; 0.694,0.511; 0.766,0.717; 0.696,0.695) (r = -0.697, -0.576); there was no correlation between the control two groups. Conclusion: MPO may be involved in the pathophysiology of PE. Increased MPO mRNA expression in placenta may be an important reason for the increase of serum MPO level. PE patients with abnormal lipid metabolism and increased insulin resistance and elevated serum levels of MPO, they may be involved in the serum MPO levels to promote the oxidative stress of PE after the pathophysiological process.